From the wound of entry, the rabies virus travels quickly along the neural pathways of the peripheral nervous system. The retrograde axonal transport of the rabies virus to the CNS (Central Nervous System) is the key step of pathogenesis during natural infection. The exact molecular mechanism of this transport is unknown although binding of the P protein from rabies virus to the dynein light chain protein DYNLL1 has been shown.[11] P also acts as an interferon antagonist, thus decreasing the immune response of the host.
From the CNS, the virus further spreads to other organs. The salivary glands located in the tissues of the mouth and cheeks receive high concentrations of the virus, thus allowing it to be further transmitted due to projectile salivation. Fatality can occur from two days to five years from the time of initial infection.[12] This however depends largely on the species of animal acting as a reservoir. Most infected mammals die within weeks, while strains of a species such as the African yellow mongoose (Cynictis penicillata) might survive an infection asymptomatically for years.[13]